Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). In pathology, the disease is characterized as scattered demyelination lesions, axonal loss and damage in both the brain and spinal cord (Lassmann, 2005), which results in a multiplicity of neurological deficits. Current therapies for managing patients with MS primarily target the inflammatory aspect of the disease (Zamvil and Steinman, 2003) and are only partly effective and limited by side effects. Recent studies suggest that glutamate-mediated cytotoxicity (excitotoxicity) (Stover et al., 1997; Barkhatova et al., 1998; Smith et al., 1999; Pitt, 2000), oxidative stress (Gilgum-Sherki et al., 2004) and mitochondrial damage (Andrews et al., 2005), may play vital roles in the pathogenesis of MS.
Measles is a member of the family Paramyxoviridae. Two types of measles virus are known, systemic measles and neural measles. While systemic measles causes the fever and rash generally associated with the measles virus. Neural measles virus is the etiology of sclerosing panencephalitis, which is an acute demyelinating disease (Sherman et al., 1965) with the pathologic characteristics of multiple sclerosis.